Over the past year, studies were performed to examine the factors which regulate the synthesis and secretion of human placental lactogen (hPL) and human decidual prolactin (hPRL). Arachidonic acid, the unsaturated fatty acid precursor of the prostaglandins and hydroperoxy fatty acids, was shown to stimulate the secretion of hPL in a dose-dependent manner. Phospholipase A2 and the fatty acid precursors of arachidonic acid also stimulated hPL secretion but other fatty acids, prostaglandins and cyclo-oxygenase and lipoxygenase inhibitors were without effect. In contrast to its effects on hPL secretion, arachidonic acid, phospholipase A2 and arachidonic acid precursors inhibited the synthesis and secretion of decidual prolactin. Prolactin synthesis and secretion, however, were unaffected by other fatty acids, prostaglandins and cyclo-oxygenase inhibitors. These studies therefore suggest that arachidonic acid may be involved in the regulation of the synthesis of hPL and the synthesis and secretion of decidual PRL. Over the next year, studies will be performed to delineate the mechanisms by which arachidonic acid affects these effects. In preliminary studies, we have demonstrated that the intravenous infusion of growth hormone or prolactin to fetal sheep has no significant effects on plasma somatomedin-C concentrations but that the infusion of oPL causes an increase in somatomedin-C concentrations. Over the next year, we plan to continue these infusion studies in both normal and hypophysectomized sheep fetuses.